Li Li

Publications (2)3.35 Total impact

• Article: Direct regulation of caspase‑3 by the transcription factor AP‑2α is involved in aspirin‑induced apoptosis in MDA‑MB‑453 breast cancer cells.

  Feng Yan, Qiongzhi He, Xiang Hu, Wen Li, Ke Wei, Li Li, Yingli Zhong, Xiaofeng Ding, Shuanglin Xiang, Jian Zhang
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  ABSTRACT: Aspirin has been reported to trigger apoptosis in various cancer cell lines. However, the detailed mechanisms involved remain elusive. The present study aimed to investigate whether aspirin plays a role in apoptosis of MDA-MB-453 cells. The effect of aspirin on the proliferation of human MDA-MB-453 cells breast cancer cells was evaluated using MTT assay, flow cytometry and western blotting. The present study reports that aspirin induces the apoptosis of MDA‑MB‑453 breast cancer cells which was attributed to the increased expression and activation of caspase‑3. Moreover, AP‑2α, a transcription factor highly expressed in MDA‑MB‑453 cells, was identified as a negative regulator of caspase‑3 transcription and AP‑2α was attenuated following aspirin treatment. Therefore, aspirin may increase the expression of caspase‑3 by inducing the degradation of AP‑2α, which increases activated caspase‑3 expression, thereby triggering apoptosis in MDA‑MB‑453 cells. Thus, aspirin may be used in breast cancer therapy.
  Molecular Medicine Reports 01/2013; · 0.42 Impact Factor
• Article: TNFAIP1 interacts with KCTD10 to promote the degradation of KCTD10 proteins and inhibit the transcriptional activities of NF-κB and AP-1.

  Xiang Hu, Feng Yan, Fangmei Wang, Zijian Yang, Ling Xiao, Li Li, Shuanglin Xiang, Jianlin Zhou, Xiaofeng Ding, Jian Zhang
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  ABSTRACT: The broad-complex, tramtrack, and bric-a-brac/poxvirus and zinc finger domain-containing protein tumor necrosis factor, alpha-induced protein 1 (TNFAIP1) was first identified as a gene whose expression can be induced by the tumor necrosis factor alpha. Some studies showed that TNFAIP1 may function in DNA replication, apoptosis and human diseases. However, the definite functions and the mechanisms of TNFAIP1 are poorly known. In this study, we performed a yeast two-hybrid assay and used TNFAIP1 as the bait to screen human brain cDNA library. Potassium channel tetramerisation domain containing 10 (KCTD10) was identified as TNFAIP1-interacting partner. The KCTD10-TNFAIP1 interaction was then confirmed by the in vitro GST pull-down assays and the in vivo co-immunoprecipitation and colocalization assays. In addition, protein degradation and ubiquitin assays revealed TNFAIP1 overexpression resulted in ubiquitin-mediated degradation of KCTD10 proteins, which was significantly alleviated with the proteasome inhibitor MG132 treatment. Furthermore, transient transfection assays with two reporters showed that TNFAIP1 and KCTD10 inhibited the transcriptional activities of nuclear factor kappa B (NF-κB) and activating protein-1 reporters. Taken together, our results indicated the novel interaction and function between KCTD10 and TNFAIP1 in human PDIP1 family.
  Molecular Biology Reports 07/2012; 39(11):9911-9. · 2.93 Impact Factor